IntroductionWith the failure of high-density lipoprotein (HDL) cholesterol raising therapies to reduce cardiovascular risk, attention has turned towards HDL composition and function. There are several techniques for the isolation of lipoproteins from plasma, with density ultracentrifugation considered the gold-standard method. It is not known which form of density ultracentrifugation is optimal for HDL composition and function analyses.MethodsThis study compared HDL composition by nLC-MS/MS and ELISA, subclass distribution by gel electrophoresis, and in vitro vascular anti-inflammatory function in HDL fractions isolated by sodium bromide sequential density ultracentrifugation (SDU) and iodixanol density gradient ultracentrifugation (DGU).ResultsHDL composition differed between the two isolation techniques, with DGU-isolated HDL fractions containing a higher total protein content than SDU (10.14 ± 1.49 mg/mL compared to 3.18 ± 1.10 mg/mL respectively, p < 0.001, mean ± SD) but lower proteomic detection of key HDL proteins such as apolipoprotein A-I, apolipoprotein A-II and paraoxonase-1 in DGU-isolated HDL. HDL subclass distribution could not be determined in DGU HDL fractions due to contaminating plasma proteins. Vascular anti-inflammatory function was higher in DGU HDL (77.5 ± 4.4 % compared to 58.3 ± 4.8%, mean ± SD, p = 0.014) possibly due to the presence of confounding plasma proteins.ConclusionFurther steps may need to be added to DGU methods to obtain a ‘cleaner’ HDL fraction and therefore currently SDU is better suited to studies of HDL composition and function.

OBJECTIVES:There is a lack of knowledge about whether occupational exposures increase the risk of emphysema, especially in never-smokers. Our objective was to determine if occupational exposures are associated with emphysema and impaired diffusing capacity. METHODS:In the Swedish CArdioPulmonary bioImage Study (SCAPIS), persons from the general population aged 50-64 answered a questionnaire and underwent CT of the lung as well as assessment of the diffusing capacity of their lungs for carbon monoxide (DLCO), presented as DLCO<lower limit of normal (LLN). Emphysema was defined as emphysema in any part of the lungs. Occupational exposures were assessed by a job exposure matrix based on longest held job. ORs with 95% CIs were calculated using logistic multivariable models. RESULTS:In this cross-sectional study (27 370 persons including 13 981 never-smokers), occupational exposure to inorganic dust was associated with emphysema (OR 1.25, 95% CI 1.07 to 1.47), also among never-smokers, (OR 1.46, 95% CI 1.00 to 2.11). There were associations with DLCO<LLN for occupational exposure to inorganic dust and vapour and gases. With all exposures in the same model, inorganic dust was associated with emphysema (OR 1.30, 95% CI 1.08 to 1.57), and vapour and gases were associated with DLCO<LLN (OR 1.17, 95% CI 1.00 to 1.38). In those with emphysema and impaired DLCO, there was an association with inorganic dust (OR 1.65, 95% CI 1.20 to 2.28), also among never-smokers (OR 3.79, 95% CI 1.35 to 10.63). CONCLUSIONS:Occupational exposures to inorganic dust are associated with emphysema. The association is stronger in those with the combination of emphysema and impaired DLCO indicating serious exposure effects in the alveoli.

BACKGROUND:Studies on long-term exposure to air pollution at high levels suggest an association with increased risk of metabolic syndrome (MetS). We aimed to study this relationship at very low levels, less well-studied, yet of public health importance. METHODS:The Swedish CArdioPulmonary bioImage Study (SCAPIS) consists of randomly selected subjects aged 50-64 years from six large cities in Sweden (n = 30,154). Participants underwent medical examination and answered a health-related questionnaire at enrolment. MetS was defined using established criteria. Residential exposure to PM2.5 and NO2 was modelled annually for each subject over 10 years before enrolment. Adjusted prevalence ratios (adj PR) were calculated both by quartiles of exposure and per 1 μg/m3 increment in PM2.5 and NO2, with adjustments for age, lifestyle and socioeconomic factors. RESULTS:Full information on exposure, covariates, and MetS was obtained for 13,997 (90.26 %) females and 12,978 (88.61 %) males, respectively. The 10-years mean exposures of PM2.5 and NO2 before enrolment were 6.57 and 11.47 μg/m3, respectively. The prevalence of MetS was 28.75 % in females and 38.20 % in males, respectively. Quartile analysis of PM2.5 did not reveal significant increased adj PR for MetS, neither in females nor in males. For females the adj PR per 1 μg/m3 was 0.91 (0.89-0.94) and for males 0.95 (0.92-0.97), respectively. Similar, but somewhat weaker, associations were seen for NO2. CONCLUSION:Some inverse associations between air pollution and MetS were observed, but these results should be interpreted with caution due to limitations in the cross-sectional design. Results should not be interpreted beyond our studied exposure range.

Introduction:Neuroinflammation and oxidative dysfunction, and their reciprocal interplay, are critically involved in the pathophysiology of chronic neuropathic pain (NeuP). Numerous studies have investigated the crosstalk between inflammatory biomolecules such as cytokines, chemokines, and neuronal cells. However, the impact of immunomodulatory lipoproteins and oxylipins in NeuP pathophysiology is far less explored. Methods:Using a combination of techniques, we uncovered altered lipoprotein composition in high-density lipoproteins (HDLs) and low-density lipoproteins (LDLs) with complementary alterations in the plasma profile of oxylipins and cytokines among patients. Results:Lower level of apolipoproteins in patient HDL and 2 isoforms of acute phase serum amyloid A (SAA) with higher levels in patients was found. The constitutively expressed SAA4 was detected in 6 isoforms in patients, but only 2 isoforms were detected in healthy controls. In LDL, lysozyme C and 2 isoforms of SAA were exclusive to patients. Analysis of protein carbonylation showed oxidation of 6 proteins in HDL, of which 3 were unique to patients. No oxidized proteins were observed in LDL. Oxylipin analysis revealed 13 octadecanoids that were significantly downregulated in patients, of which 7 demonstrated significant activating effects on the Kv7.2/7.3 channel, which is anticipated to dampen neuronal signalling in sensory afferents. Among the significant octadecanoids, 9-HODE showed most prominent facilitating effects on Kv7.2/7.3 channel activation. Conclusion:These results present a previously unexplored network of integrated alterations of lipoproteins, octadecanoids, and cytokines in patients suffering from NeuP, indicative of deviant immuno-protective functioning across several biological systems including lipid metabolic processes, inflammation, and Kv7.2/7.3 signalling.

Background Exposure to hexavalent chromium (Cr(VI)) can occur during occupational activities and leading lung cancer. MicroRNA (miRNA) plays an important part in carcinogenesis. Whether Cr(VI) exposure causes cancer-related miRNA changes is yet uncharacterized. Methods This study included 89 Cr(VI) exposed workers and 47 controls. MiRNAs were extracted from plasma followed by library preparations, miRNA sequencing, and differentially expressed miRNAs (DEMs) analysis. To understand the underlying biological functions, we used bioinformatics approaches, and qPCR was performed to validate the expression of potential target genes. Results A total of 2100 miRNAs were detected. In the exposed workers, 59 DEMs were identified: 21 up-regulated and 38 down-regulated. Target genes for both up- and down-regulated DEMs were significantly enriched in: miRNAs in cancer, small cell lung cancer and non-small cell lung cancer. Protein-protein interactions showed a high number of interactions, in which CCNE2, CDK4 and E2F1 were predicted as hub genes, and the messenger RNA expression of those genes was significantly higher in the exposed workers compared with controls. Conclusions Our study suggests that low-to-moderate Cr(VI) exposure results in differential expression of lung-cancer-related miRNAs and associated target genes. Further studies are needed to validate our findings and clarify whether these changes predict cancer risk.

Background The association between socioeconomic status (SES) and environmental burden is context-dependent. Those with low SES may be more likely to live near major roads and industries where environmental exposures are high but may also be more likely to live further away from city centers. The aim of this study was to investigate the association between SES and environmental burden in Sweden. Methods The Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort recruited participants from six Swedish cities during 2013-2018. Residential environmental exposures (particulate matter <2.5 m [PM2.5], road traffic noise, and lack of greenspace) and neighborhood-level SES factors (proportions with low-income, low education, unemployment, rental units, foreign born) were assessed from participants' addresses in 2018. Individual-level SES factors (financial buffer, education, occupation, type of living, foreign born) were obtained from a questionnaire and neighborhood data from Statistics Sweden. Linear regression models were used to analyze the link between environmental exposures and SES factors. Correlations between SES factors were analyzed using Cram & eacute;r's V and Spearman rank correlations. Results The study included 23 320 SCAPIS participants in 1939 neighborhoods. The explanatory power of SES factors differed substantially between factors and cities. A model with all ten SES factors could account for 25-88 %, 36-60 %, and 49-81 % of the spatial variance in PM2.5, noise, and lack of greenspace respectively. Neighborhoods with more low-income earners, rental units and foreign born had more environmental burden. Neighborhoods with more inhabitants with low education and unemployment had less environmental burden. Associations were generally non-linear. Individual-level SES factors were not associated with environmental burdens after adjusting for neighborhood SES factors. Individual and neighborhood SES were weakly correlated. Conclusion Neighborhood SES factors accounted for a large proportion of the variance in environmental burdens, whereas individual SES factors did not. The relationship between SES and environmental burden differed greatly between indicators and cities.

Abstract Welding constitutes a source of particles and dust that effects a large number of individuals at occupational environments throughout the world. Besides being classified as a carcinogen, welding fume has potential inflammatory properties and has been linked to cardiovascular disease. We monitored the exposure at two large manufacturing companies welding in mild steel before but also after extensive preventive actions. Exposure was assessed by collecting respirable dust and its metals through stationary and personal sampling at multiple occasions over the study. Particle levels were assessed by using handheld particle-counting instruments. Both workers doing actual welding but also workers not welding themselves provided blood, urine and nasal lavage fluid for biomonitoring of potential health effects including inflammation, cardiovascular, renal and upper airways effects. The interventions provided improvement in exposure for the workers at the companies. Some interventions appeared more successful with longevity while others only provided a temporary lowering lost over time. Use of welding helmet with integrated respirators were shown to be relatively non-effective at sufficiently lowering the exposure for welders in places with poor ventilation and local exhaust ventilation. The biomonitoring provided data investigated in relation to the exposure to further our understanding of potential health effects in both welders but also workers working in close proximity to the welding processes.

Abstract Introduction Hexavalent chromium Cr(VI) is a human carcinogen, but the current exposure to Cr(VI) at Swedish workplaces is unknown. Methods Recruitment of 113 workers with potential Cr(VI) exposure and 72 controls was combined with measurements of inhalable Cr(VI) (only exposed workers) and total Cr in urine and red blood cells (RBC), Bayesian analysis of occupational exposure limit (OEL) compliance was used, as well as the Swedish job-exposure-matrix. Results Exposed workers performed processing of metal products, steel production, welding, and plating. The geometric mean concentration of inhalable Cr(VI) in exposed workers was 0.15 μg/m3. Eight workers (7%) exceeded the Swedish OEL (5 μg/m3), and the share of OEL exceedances was estimated to be up to 19.6% for stainless steel welders. Urine- and RBC-Cr were significantly higher in exposed workers compared with controls. Workers with inferred non-acceptable local exhaustion ventilation showed significantly higher inhalable Cr(VI), urine- and RBC-Cr than those with acceptable ventilation. Workers with inferred correct use of respiratory protection had higher inhalable Cr(VI), and, paradoxically, higher urine- and RBC-Cr concentrations than workers with incorrect use. We estimate that ~17 900 Swedish workers are occupationally exposed to Cr(VI) today. Discussion Our study showed that although most air measurements were relatively low, 7% exceeded the OEL, and particularly stainless steel workers are at risk for exceeding the OEL. The existing protective measures implemented at workplaces are still inadequate and insufficient. Conclusion Some workers in Sweden are exposed to high levels of the non-threshold carcinogen Cr(VI). National strategies aligned with European strategies are needed to eliminate occupational cancer.

Background and aims Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. Methods We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 mu m (PM2.5), <10 mu m (PM10), and nitrogen oxides (NOx) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. Results Median 10-year average PM2.5 exposure was 6.2 mu g/m(3) (range 3.5-13.4 mu g/m(3)). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 mu g/m(3)). Associations with significant stenoses were inconsistent. Conclusions In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.

Abstract Metal additive manufacturing (AM), commonly known as 3D-printing, is an emerging state-of-the art technology with significant economic and practical advantages. Due to its relative short history, especially in industrial serial production, the knowledge regarding exposure and health risks is severely limited. To alleviate this, we have monitored the occupational exposure and potential health effects at both smaller R&D-sites and at large-scale AM/powder production facilities. Exposure was monitored through stationary and personal sampling of total and inhalable dust followed by metal analysis. Particle counting instruments were used to identify dusty works tasks and to evaluate preventive measures. AM operators and controls underwent health examinations, including questionnaires, spirometry, and blood and urine sampling to measure exposure and clinical health markers. Exposure during printing were generally low but other aspects of the production chain were of greater concern regarding exposure risks: production of metal powder feedstock, handling of metal powder before/after print, and post-printing processes. During three research projects, we have seen a shift from a dusty work environment to a more safe-by-design approach throughout the AM process. Despite the AM operator’s relatively low exposure to dust and metals, we identified changes in a urinary marker for kidney function. However, this finding needs to be further evaluated. In summary, our studies into the relative new field of metal AM exposure and health effects provides a basis to help companies and operators handling these techniques to move toward safe working conditions.

Given the failure of high-density lipoprotein (HDL) raising therapies to reduce cardiovascular disease risk, attention has turned towards HDL composition and vascular protective functions. In individuals with insulin resistance, exercise interventions recover HDL function. However, the effect of exercise on HDL in otherwise healthy individuals is unknown. This cross-sectional study aimed to measure HDL composition and antioxidant/endothelial anti-inflammatory function in insulin sensitive endurance athlete and healthy control men. HDL was isolated using density gradient ultracentrifugation. HDL composition was measured using microplate assays for apolipoprotein A-I, total cholesterol content and apolipoprotein M. HDL protein composition was measured using nano-liquid chromatography tandem mass spectrometry. HDL subclass distribution was measured by native gel electrophoresis. HDL in vitro antioxidant function was measured by paraoxonase-1 activity assay and anti-inflammatory function assessed in endothelial cells. Compared with controls, endurance athlete HDL had higher apolipoprotein A-1 (1.65 ± 0.62 mg/ml vs 1.21 ± 0.34 mg/ml, P=0.028) and higher total cholesterol content (2.09 ± 0.44 mmol/L vs 1.54 ± 0.33 mmol/L, P<0.001). Proteomics revealed higher apolipoprotein A-II, A-IV and D and transthyretin in endurance athlete HDL versus controls. There was no difference observed in in vitro HDL antioxidant or anti-inflammatory functions between controls and endurance athletes. Despite a more favourable composition, endurance athlete HDL did not have higher in vitro antioxidant or anti-inflammatory function. It is possible that HDL has a ceiling of function, i.e. that healthy HDL function cannot be enhanced by endurance exercise.

Abstract Background Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers. Methods We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM2.5), inhalable particulate matter (PM10), and nitrogen oxides (NOx) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders. Results Median long-term PM2.5 exposure was 6.2 µg/m3. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m2. PM2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m3 (interquartile range, IQR). PM2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m3. There was a tendency towards an association between PM10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent. Conclusion In this large general population sample at low exposure levels, we found a surprising association between PM2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.

Environmental pollution is of global concern. In Southeast Sweden, historical glass production has contaminated communities with toxic metals. Long-term residency in these communities and high consumption of local foods may constitute a risk for cardiovascular disease (CVD) or stroke.The current study investigates if residency in these contaminated sites and long-term consumption of local foods is associated with self-reported CVD and stroke. In addition, the body burden of the toxic metals arsenic, cadmium, and lead, as well as inflammatory protein markers, were studied for association with CVD and stroke.From an existing questionnaire cohort and biomonitoring sub cohort (n = 2290/882) of people living in the contaminated areas, self-reported CVD cases (n = 366/166) and stroke cases (n = 78/25) were identified. Individuals were grouped based on their residency within a 2 km radius of glassworks with historical high, moderate, or low air-borne lead emissions. Body burden of arsenic, cadmium, and lead was analyzed using ICP-MS. Inflammatory markers were investigated using electrochemiluminescence.Long-term residency near glassworks with historically high levels of lead emissions, and high consumption of local foods, were associated with CVD. The risk was increasing for each year of residency in high emission areas. Increased body burden of arsenic in blood, and lead in urine, were associated with stroke. Five and two inflammatory markers, respectively, were elevated in CVD and stroke cases after adjusting for confounders.An increased risk for CVD was found in areas with historically high emissions of lead but possibly also other toxic metals. Interestingly, there was an indication of a dose-response relationship with increasing risk for CVD per year of residency time. Inhalation and consumption of local food may constitute major pathways for this association. The study shows that long-term exposure to toxic metals in these contaminated areas is associated with CVD and that there is a need to limit exposure in the general population.

The objective of the present study was to assess historical emissions of Pb to air around a number of glassworks sites in southeastern Sweden, and the possible implications for human exposure. To do so, a four-step method was applied. First, emissions of Pb to air around 10 glassworks were modelled for the 20th century. Second, an assessment of the resulting exposure was made for a number of scenarios. Third, the number of people potentially exposed at different times was estimated, and fourth, measurements of "current" Pb concentrations in PM10 material from four sites were conducted in 2019. The results show that the highest emissions, and exposures, occurred from 1970 to1980. It coincides with the time period when the highest number of people resided in the villages. At this time, the average Pb concentration in air around the six largest factories was about 2.4 μg Pb/m3, i.e. 16 times the present US national ambient air quality standard (NAAQS) of 0.15 μg Pb/m3. By year 2000 the modelled average concentration had dropped to 0.05 μg Pb/m3, a level that is normal for urban regions today. The PM10 measurements from 2019 indicate a further decline, now with a mean value of about 0.02 μg Pb/m3. Over the entire study period, inhalation hazard quotients (HQs) exceeded the dietary HQ by many orders of magnitude, indicating that inhalation has been the most prevalent exposure pathway in the past. At present, both pathways are judged to be associated with low exposures. Even if only roughly approximated, a picture of the historical exposure can increase our understanding of the connection between exposure and disease, and can be valuable when risks are to be communicated to residents near contaminated areas.

The dominant road traffic particle sources are wear particles from the road and tire interface, and from vehicle brake pads. The aim of this work was to investigate the effect of road and brake wear particles on pulmonary function and biomarkers in isolated perfused rat lungs. Particles were sampled from the studded tire wear of three road pavements containing different rock materials in a road simulator; and from the wear of two brake pad materials using a pin-on-disk machine. Isolated rat lungs inhaled the coarse and fine fractions of the sampled particles resulting in an estimated total particle lung dose of 50 μg. The tidal volume (TV) was measured during the particle exposure and the following 50 min. Perfusate and BALF were analyzed for the cytokines TNF, CXCL1 and CCL3. The TV of lungs exposed to rock materials was significantly reduced after 25 min of exposure compared to the controls, for quartzite already after 4 min. The particles of the heavy-duty brake pads had no effect on the TV. Brake particles resulted in a significant elevation of CXCL1 in the perfusate. Brake particles showed significant elevations of all three measured cytokines, and quartzite showed a significant elevation of TNF in BALF. The study shows that the toxic effect on lungs exposed to airborne particles can be investigated using measurements of tidal volume. Furthermore, the study shows that the choice of rock material in road pavements has the potential to affect the toxicity of road wear PM10.

The increasing use of additive manufacturing (AM) techniques (e.g., 3D-printing) offers many advantages but at the same time presents some challenges. One concern is the possible exposure and health risk related to metal containing particles of different sizes. Using the nickel-based alloys Hastelloy X (HX) and Inconel 939 (IN939) as a case, the aim of this cross-disciplinary study was to increase the understanding on possible health hazards and exposure. This was done by performing in-depth characterization of virgin, reused and condensate powders, testing in vitro toxicity (cytotoxicity, genotoxicity, oxidative stress), and measuring occupational airborne exposure. The results showed limited metal release from both HX and IN939, and slightly different surface composition of reused compared to virgin powders. No or small effects on the cultured lung cells were observed when tested up to 100 µg/mL. Particle background levels in the printing facilities were generally low, but high transient peaks were observed in relation to sieving. Furthermore, during post processing with grinding, high levels of nanoparticles (> 100,000 particles/cm3) were noted. Urine metal levels in AM operators did not exceed biomonitoring action limits. Future studies should focus on understanding the toxicity of the nanoparticles formed during printing and post-processing.

BACKGROUND AND AIM: Despite firm evidence for an association between long-term air pollution exposure and cardiovascular events also at low exposure levels, previous epidemiological studies on the association with atherosclerosis have been inconsistent. The aim of this study was to investigate associations between long-term low-level air pollutant exposure and coronary atherosclerosis. METHOD: We performed a cross-sectional analysis in the large Swedish CardioPulmonary bioImaging Study (SCAPIS, n = 30 154). Men and women 50–64 years old were recruited from the general population of six Swedish cities 2013–2018. Outcomes were coronary atherosclerosis (segment involvement score, SIS), coronary artery calcium score (CACS), and non-calcified coronary plaque (NCP) prevalence. Hourly total and source-specific residential PM2.5, PM10, and NOx were modelled in dispersion models with high spatial resolution and averaged over 10 years before recruitment. Prevalence odds ratios (POR) were estimated with ordinal logistic regression models adjusted for site and known risk factors, based on a directed acyclical graph. RESULTS: Median PM2.5 exposure was 6.2 µg/m3; 44% of participants had detectable coronary atherosclerosis. PM2.5 was not associated with SIS or CACS, but with a higher NCP prevalence (POR 1.65, 95% CI 1.18, 2.31, per interquartile range [2.05 µg/m3] higher PM2.5) with a dose-response pattern (p = 0.034 for linear trend). Other pollutants and source-specific exposures did not demonstrate consistent positive associations with any of the outcomes. CONCLUSIONS: In this large, middle-aged general population sample at low exposure levels, PM2.5 exposure was not associated with estimates of general coronary atherosclerosis or calcification, yet appeared to be associated with non-calcified plaques, which may reflect an association with the early phase of atherosclerosis or more vulnerable forms of atherosclerosis. The main funder of SCAPIS is the Swedish Heart and Lung Foundation. Funding for this study was provided by the Swedish Research Council for Health, Working Life and Welfare (FORTE).

Abstract Welding fume constitutes a source of particles and dust that effects a large number of individuals at occupational environments throughout the world. Besides being classified as a carcinogen, welding fume has potential inflammatory properties and has been linked to cardiovascular disease. To further increase the knowledge regarding potential health and inflammatory effects, workers at occupational environments with exposure to welding fume were investigated before but also after extensive preventive actions to investigate potential effects that may be pathways for cardiovascular disease. Exposure was assessed by collecting respirable dust through stationary and personal sampling at multiple occasions over the study. Dust was used for metal analysis by ICP-MS. Particle levels were assessed by using three handheld particle-counting instruments, Lighthouse 3016-IAQ (0.3-10 µm), DustTrak 8520 (0.1-10µm) and Philips Aerasense NanoTracer (10-300 nm). A total of approximately 100 individuals were screened at the beginning and end of a workweek at the beginning of the study and again after two years after the companies had introduced a wide range of preventive actions to reduce the exposure of the workforce. Participants had metals measured in both blood and urine, markers used in clinical practice for stress in different tissues were measured, lung function using spirometry was done and a set of 40 different acute inflammatory markers were measured using electrochemiluminiscence. The study adds to the growing knowledge of effects of welding fumes on human health and how preventive actions may affect this.